Renal Flashcards

1
Q

Kidney function

A

homeostasis of internal environment
maintenance of fluid and electrolyte balance
secretion of EPO, renin, dihydroxy Vit D

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2
Q

Renal Capsule

A

tightly adhering capsule covers outer surace

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3
Q

renal cortex

A

major components include the glomeruli and portion of tubules

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4
Q

renal medulla

A

proximal/distal tubules
collecting ducts
renal pyramids

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5
Q

calyces

A

recieve urine from the large collecting ducts, have smooth muscle that contracts to move urine into the bladder

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6
Q

Minor/major Calyx

A

apex of pyramids project into a cup-shaped cavity, join together to form major calyx to join together to form the RENAL PELVIS

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7
Q

Nephron

A

selective reabsorption and secretion of ions & mechanical filtration of fluid,waste,electrolytes
regulation of acid/bases

3 types

  • superficial cortical
  • midcortical
  • juxtadullary
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8
Q

juxtaglomerular cells

A

surround the afferent artery where it enters the glomerulus

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9
Q

Juxtaglomerular apparatus

A

it controls renal blood flow, glomerular filtration, renin secretion

filtrates plasma and removes wastes but retains water/solutes

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10
Q

Parts of the nephron

A

glomerulus- production of filtrate

PCT- reabsorption of water ions and all organic nutrients

Loop of henle- further reabsorption of water (descending) and Na+ Cl- (ascending)

DCT- secretion of ions, acids, drugs, toxins, variable reabsorption of water, Na+ ions, Ca+ ions

Collecting duct- variable reabsorption of water, sodium, potassium, hydrogen bicarbonate

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11
Q

Glomerular filtration membrane

A

separates blood in the glomerular capillaries from the fluid in the bowmans space

allows all the components of blood to filter through except blood cells, plasma proteins, negatively charged proteins

releases vasodilation and vasoconstriction to regulate blood flow

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12
Q

Glomerular filtration rate

A

filtration of plasma per unit of time
degree of renal function
loss or damage to nephrons lead to decrease in GFR
normal rate 90-125 mL/min

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13
Q

renal clearance

A

vol of blood plasma cleared of a waste product in 1 minute

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14
Q

Rate of filtration depends on

A
  • pressure across different/efferent arterioles
  • pressure across glomerular capillaries
  • pressure inside bowmans capsule
  • changes in hydrostatic pressure
  • changes in diameter of arterioles
  • large molecules cannot move through small pores in glomerular membrane
  • negative charge along filtration membrane, negatively charged particles get repelled
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15
Q

Renin-angiotensin-aldosterone system (RAA)

A

ADH are the feedback loop systems maintaining homeostasis within the body

Hypothalamus releases ADH
increase in nephron permeability
additional water is absorbed
serum osmolarity normalised
ADH release stops
increase serum osmorlarity
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16
Q

Aldosterone

A

regulation of BP, acts on distal tubules & collecting duct
keeps pressure in glomerulus within a wide range of system BP

so blood flow & GFR are constant over a range of pressure 80-180

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17
Q

Renal function tests

A
  • measured by amount of renal clearance
  • amount of a substance that can be cleared from the blood by the kidneys

C= UV/P
u- rate of urine output
v- urine output
p- waste concentration in plasma

an indirect measure of GFR, tubular secretion, tubular reabsorption, renal blood flow

can measure creatine and insulin

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18
Q

creatine

A

produced by muscle
released into blood at relatively constant rate
filtered by the glomerulus
clearance overstimulates GFR

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19
Q

Anuria

A

no urine production

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20
Q

Oliguria

A

decrease urine production

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21
Q

Polyuria

A

excessive and abnormal urine production

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22
Q

Diuresis

A

increase urine production

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23
Q

Nocturia

A

urine production at night

24
Q

Haematuria

A

blood in urine

25
Q

Azotaemia

A

increase blood urea, indicates renal dysfunction

26
Q

Uraemia

A

above and other electrolyte/metabolic abnormalities

27
Q

Obstructive Uropathy

A

Any condition,structural or functional, causing a change in the normal urine flow anywhere within urinary tract
causes vary with age and gender

causes
pain- distention caused by blockage
urine output- can vary depending on degree of blockage
hypertension- (unilateral) - increase renal secretion
(bilateral)-extracellular fluid vol expansion

28
Q

partial vs complete obstruction

A

partial- compression and accumulation of urine, ischaemic damage and atrophy with decrease concentrating ability of the kidney

complete- Decrease GFR, resulting in renal failure

29
Q

hydroureter + hydronephrosis

A

hydroureter =obstruction of ureter with accumulation of urine

hydronephrosis= increase in hydrostatic pressure in renal pelvis, calyces increase accumulation of urine in renal collecting system

renal tubules affected first, impaired concentration, decrease GFR
kidneys enlarge, pelvis/calyces dilated, calyces blunted
cortical tubules lost-interstitual fibrosis\

ss
pain
bladder symptoms

types
bilateral (partial)- poluria, nocturia, acidosis, HT
bilateral (complete)- oliguria, anuria
unilateral - asymptomatic

30
Q

Kidney stones patho

A

changes in pH and temp
decrease in urinary flow
high urinary concentration of stone forming substance
grow in renal papilla + pelvis

31
Q

calcium kidney stone

A
smallest
hypercalciuria
hyperuricosuria
bone demineralisation
diet high in vegetables
prolonged mobility
hyperparathyroidism
middle aged men with a family history
32
Q

struvite kidney stone

A

women infected by microbes

alkaline urine

33
Q

Uric acid stone

A

acidic environment can cause

  • ulcerative colitis/ regional enteritis with fluid/ bicarbonate loss
  • sufferers with gout, high meat and fish diets
  • leukaemia
34
Q

Cysteinuria

A

rare hereditary disorder
disorder of amino acid metabolism
decrease tubular reabsorption of cysteine

SS
pain, flank pain, nausea and vomiting, haematuria

predisposing factors
family history, diabetes, pregnancy, childhood infection, chronic disease, immunosupression, renal calculi, UT obstruction, prostate disease in older men

treatment
adequate analgesia, surgical removal of stones
treat infection
dissolve stones, prevent formation

35
Q

Patho of Cysteinuria

A

high level of stone forming substance in plasma and urine
high pH favours struvite and deposition of Ca2+ with oxalate, phosphates, carbonates
low pH favours uric acid stones
decrease urine output and high concentration

found in papillae, renal tubules, calyces or pelvis, most

36
Q

Kidney Dysfunction

A
  1. Inadequate urine production
  2. homeostasis severly impaired
    - fluid, electrolyte, acid-base balance
    - accumulation of creatinine, urea
    - decrease excretion of drug metabolism
    - inadequate reabsorption of amino acids, glucose
  3. impaired conversion of Vit D
    - to the active form
    - impaired Ca2+ absorption
  4. impaired secretion of erythropoietin
    - decrease RBC production
    - decrease oxygen carrying capacity of blood in bone marrow, decrease bone mineralisation
37
Q

Glomerulonephritis (GMN)

A

inflammation of the glomerulus
major cause of chronic kidney disease
reduction 30-50% reduction of GFR- end stage renal failure

primary= rapidly progressive glomerulonephritis
e.g IgA neuropathy

secondary= secondary to other diseases
e.g diabetes, SLE, malaria, solid tumors

38
Q

Patho of GMN

A

damage to glomerulus
swelling, increase in permeability
large protein molecules and RBC are filtered and seen in urine
swelling, increase in pressure, decrease GFR
causes systemic edema, HT

epithelial layer of glomerular capillary membrane is disturbed
change in permeability, basement membrane thickens
occurs as a consequence of activation and release of a variety of mediators

39
Q

5 types of GMN

A
  1. Asymptomatic
  2. Acute Nephritic syndrome
  3. Rapidly progressive GMN
  4. Nephrotic syndrome
  5. Chronic Glomerulonephritis
40
Q

Asymptomatic (IgA nephropathy)

A

most common form of GMN,
young men, 15-30 year old
-abnormal IgA binds to cells, complement stimulates inflammation & injury
-40% show assymptomatic haematuria

41
Q

Acute Nephritic syndrome

A

group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney or glomerulonephritis

ss
acute onset of gross haematuria, oliguria, mild-moderate proteinuria, increase creatine, HT, mild oedema, RBC/WBC in urine

42
Q

Acute post-streptococcal glomerulonephritis (GMN)

A

circulating antibody- antigen complexes deposited in glomeruli
complement activate inflammation
WBC infiltrate & glomerular cells proliferate
capillary blocked so filtration rate drops

ss
acute onset of fever, malaise, nausea, oliguria, haematuria, RBC in urine, mild HT, periorbital oedema

treatment
no specific treatment

43
Q

Rapidly progressive GMN

A
  • acute nephritis with glomerular damage
  • results in proteinuria
  • rapid progression to AKI with severe oliguria, anuria and irreversible kidney disease after weeks- months
  • 50-60 years

extensive proliferation of cells into bowmans space
injury is assoc by rapid decrease in glomerular function
progression to renal failure, haematuria

44
Q

Nephrotic syndrome

A

heavy protein loss
generalised oedema characterised by pitting in the legs

patho
damage/ alteration to glomerular basement/membrane
becomes permeable to plasma proteins
decrease oncotic pressure of blood, fluid remains in tissures- edema
release of inflamm mediators- thickening of walls/renal fibrosis

treatment
decrease salt, low fat diet, diruetics, immunosupression

45
Q

Chronic Glomerulonephritis (CKD)

A

encompasses glomerular diseases with a progressive course leading to chronic kidney diseases

46
Q

Acute Kidney Injury (AKI)

A

rapid/sudden deterioation of renal function resulting in retention of metabolic wastes
impaired fluid/electrolyte balance

ss
decrease urine output
increase blood urea nitrogen
increase serum creatinine
usually reversible
47
Q

Causes of AKI

A

prerenal- impaired blood flow, hypotension, ischaemia, decrease CO, haemorrhage, surgery

intrarenal- acute glomerulonephritis or acute tubular necrosis

postrenal- urinary tract obstruction

48
Q

3 stages of AKI

A
1. INITATION PHASE
decrease perfusion, oliguria
prevention of injury, lasts 1-3 weeks
fluid retention/oedema, nausea/vom
poor wound healing, fatigue
2. MAINTENANCE PHASE
period of established renal injury/dysfunction
may last weeks/months
lowest urine output
increase creatinine, BUN

3.RECOVERY PHASE
when injury is repaired, normal renal function re-established
decrease serum creatinine, urea
returning to normal function can take 3-12 months, 30% do not fully recover
diruesis common

49
Q

Chronic Kidney disease

A

gradual loss of nephrons until remainder cannot carry out normal renal function
slow but irreversible, results in end-stage renal disease
requires dialysis and maintenance for survival
GFR

50
Q

5 stages of chronic kidney disease

A
  1. KIDNEY DAMAGE+ NORMAL GFR
    GFR 75%
    evidence of kidney damage, without GFR
    HT common, start to see abnormalities in composition of urine,structural changes e.g scarring
2. MILD KIDNEY DAMAGE
GFR 50%
asymptomatic
evidence of damage in urine
subtle rise of plasma, creatinine, urea
  1. MODERATELY DECREASE GFR, MODERATE KIDNEY DAMAGE
    GFR 30-50%
    asymptomatic-mild symptoms e.g HT
    ss
    mild increase in creatinine, urea
    anaemia, polyuria, nocturia, hypovolaemia, dehydration
  2. SEVERELY REDUCED GFR
    GFR 10-25%,
51
Q

UTI

A

inflammation of urinary tract caused by bacteria from gut flora
classified according to location

predisposing factors
age, pregnancy, medical procedures, diabetes, chemotherapy, tumors, antibiotics

52
Q

acute pyelonephritis

A

upper urinary tract, calyces, medulla
usually E. Coli
increase neutrophils in tubules
usually occurs because of spread from ureter, may also occur due to blood borne diseases
can permanently damage tubules- renal damage

ss
fever, chills, flank pain, proteinuria, pyuria, hematuria, generalised malaise

53
Q

chronic pyelonephritis

A

chronic renal inflammation
severe scarring around calyces, renal pelvis, tubules
destruction of tubules, atrophy, dilation, scarring
impaired urine conc ability

ss
dehydration, hyperkalemia, metabolic acidosis, HT, flank pain, dysuria

54
Q

Renal cell carcinoma

A

malignancy of renal tubular/ductal cells
slow growing, can reach a big size before being detected as there is room to grow and the other kidney can function

metatisies early to lungs, lymph nodes and bone
can grow into vein and renal pelvis

ss
haematuria, fever, weakness, weight loss, HT, cushing syndrome, hepatic dysfunction, hypercalcaemia, malaise

55
Q

Wilms tumor- nephroblastoma

A

sporatic
genetic mutation,present with enlarged abdomen
large mass can occur anywhere in kidney, grow/distort kidney structure

ss
large abdo mass, HT, pain, vomiting, haematuria

56
Q

Bladder tumors (transitional cell carcinoma)

A

line the inner surface of bladder, urethra, ureter
metastasis via lymphatics to liver, lungs, bone marrow
has the tendency to reoccur

ss
haematuria, dysuria,

risk factors
men>60, tobacco smokers, industrial exposure to dyes, leather paint, radiotherapy, analgesic use

prognosis depends on stage its found

57
Q

mx of renal patients

A
  • if pt meets guidelines for fluid give it to them
  • morphine is okay in moderate amounts for things such as pain relief
  • rapid transport

ss to watch for

  • sudden changes in mental status/mood
  • nausea/vom/ diarrhoea
  • rapid onset of HT, oedema in feet/hands
  • rapid onset of numbness,tingling
  • seizure, muscle twitching
  • changes in ECG

pay close attention to history of illness and timing of physical findings

ask about output, and colour